RACK1对肺腺癌A549细胞生物学行为及相关蛋白表达的影响
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摘要
目的研究RACK1基因沉默对A549细胞生物学行为的影响,探究其对VEGF、Bcl-2表达的影响。方法转染RACK1 sh RNA至A549细胞,分别设稳定转染的实验组、阴性对照组和空白对照组。Western blot检测各组细胞RACK1、VEGF、Bcl-2的表达,平板克隆实验检测各组细胞的增殖情况,划痕愈合实验观察细胞运动迁移的改变,流式细胞术分析细胞凋亡率的变化。结果实验组细胞增殖能力下降,迁移能力减弱,凋亡率增高,VEGF、Bcl-2表达下调(P<0.05)。结论 RACK1基因沉默能抑制A549细胞的增殖和迁移,诱导其凋亡,下调VEGF、Bcl-2的表达。
Objective To investigate the effect of silencing RACK1 on A549 cell proliferation and VEGF,Bcl-2 expression. Methods The sh RNA was transfected into A549 cells as the experiment group. The expression level of RACK1,VEGF,Bcl-2 were measured by western blot,cell proliferation was detected by plate colony forming assay. scratch healing experiment was used to detet migration capacity. Cell apoptosis was measured by flow cytometry. Results The ability of proliferation and the migration ability of the cells in the experimental group was weakened. The apoptotic rate was increased. The expression level of VEGF and Bcl-2 were decreased. Conclusion Targeting to inhibit RACK1 expression in A549 cells could inhibit proliferation and induce apoptosis,specifically decreased the expression level of VEGF and Bcl-2.
Objective To investigate the effect of silencing RACK1 on A549 cell proliferation and VEGF,Bcl-2 expression. Methods The sh RNA was transfected into A549 cells as the experiment group. The expression level of RACK1,VEGF,Bcl-2 were measured by western blot,cell proliferation was detected by plate colony forming assay. scratch healing experiment was used to detet migration capacity. Cell apoptosis was measured by flow cytometry. Results The ability of proliferation and the migration ability of the cells in the experimental group was weakened. The apoptotic rate was increased. The expression level of VEGF and Bcl-2 were decreased. Conclusion Targeting to inhibit RACK1 expression in A549 cells could inhibit proliferation and induce apoptosis,specifically decreased the expression level of VEGF and Bcl-2.
引文
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[4]Shi S,Deng YZ,Zhao JS,et al.RACK1 promotes NSCLC tumorigenicity through activating SHH signaling pathway[J].J Biol Chem,2012,287(11):845-858.
[5]赵敏.肺癌组织芯片中STAT3,Bcl-2和VEGF表达的生物学意义及相关分子机制的研究[D].天津:天津医科大学,2006.
[6]闫凌丽,王鸿程,朱晨.STAT3信号转导途径在肺腺癌细胞中的表达活化[J].细胞与分子免疫学杂志,2009,25(2):141-142.
[7]马晓丽,孙海基,汪运山,等.胃癌组织中Sonic Hedgehog和vegf表达及临床意义的研究[J].中华肿瘤防治杂志,2007,14(24):1879-1881.
[8]Yang Q,Shen SS,Zhou S,et al.STAT3 activation and aberrant ligand-dependent SHH signaling in human pulmonary adenocarcinoma[J].Exp Mol Pathol,2012,93(2):227-236.